A method for treating skin, reducing oxidative damage to a skin cell, reducing lipoxygenase (LO) activity in a skin cell, reducing cyclooxygenase (COX) activity in a skin cell, reducing tumor necrosis factor alpha (TNF-.alpha.) in a skin cell, or reduction matrix metalloproteinase enzyme activity in a skin cell comprising contacting skin or a skin cell with an aromatic skin-active ingredient.

Walke; Bob

Gomez; Cristie

Florence; Tiffany C.

Hines; Michelle D.

Mary Kay Inc.

Methods of treating skin with aromatic skin-active ingredients

Treatment of cells with ionizing radiation is associated with the production of arachidonic acid. Inhibition of phospholipase A2 abolishes radiation-mediated arachidonate production, protein kinase C induction and tumor necrosis factor gene expression. The addition of inhibitors of lipoxygenase, such as ketoconazole, prior to irradiation reduces the expression of of tumor necrosis factor while maintaining the expression of other radiation inducible genes, such as Egr-1 and c-jun. In contrast, indomethacin, an inhibitor of cyclooxygenase, enhanced the expression of tumor necrosis factor as well as other radiation inducible genes. The results show that lipoxygenase inhibitors are useful in the treatment of radiation-induced mucositis, dermatitis, pneumonitis, proctitis, and esophagitis. which may be due to the production of cytokines such as TNF.

lipoxygenase/necrosis

Methods of treating skin with aromatic skin-active ingredients

Regulation of x-ray mediated gene expression

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